Ischemia and reperfusion-from mechanism to translation

被引:3300
作者
Eltzschig, Holger K. [1 ]
Eckle, Tobias [1 ]
机构
[1] Univ Colorado, Dept Anesthesiol, Mucosal Inflammat Program, Aurora, CO 80045 USA
基金
美国国家卫生研究院;
关键词
ELEVATION MYOCARDIAL-INFARCTION; PERCUTANEOUS CORONARY INTERVENTION; HANGING-WEIGHT SYSTEM; FIND-ME SIGNAL; T-CELLS; NITRIC-OXIDE; IN-VIVO; NUCLEOTIDE PHOSPHOHYDROLYSIS; ECTO-5'-NUCLEOTIDASE CD73; INTERMITTENT HYPOXIA;
D O I
10.1038/nm.2507
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Ischemia and reperfusion-elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea. Ischemia-reperfusion injury is also a major challenge during organ transplantation and cardiothoracic, vascular and general surgery. An imbalance in metabolic supply and demand within the ischemic organ results in profound tissue hypoxia and microvascular dysfunction. Subsequent reperfusion further enhances the activation of innate and adaptive immune responses and cell death programs. Recent advances in understanding the molecular and immunological consequences of ischemia and reperfusion may lead to innovative therapeutic strategies for treating patients with ischemia and reperfusion-associated tissue inflammation and organ dysfunction.
引用
收藏
页码:1391 / 1401
页数:11
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